We used oligonucleotide microarrays to address the specificities of transcriptional responses of adult Drosophila to different stresses induced by paraquat and H2O2, two oxidative stressors, and by tunicamycin which induces an endoplasmic reticulum (ER) stress. Flies were tested 24 hours after exposure to continuous stresses induced by ingestion of paraquat, H2O2 or tunicamycin at concentrations leading to similar effects on viability. We used concentrations of 1% H2O2, 5mM paraquat and 12uM of tunicamycin which lead to negligeable mortality at 24 hours. A paraquat concentration of 15mM was also used for comparison with previous studies Both specific and common responses to the three stressors were observed and whole genome functional analysis identified several important classes of stress responsive genes. Within some functional classes, we observed large variabilities of transcriptional changes between isozymes, which may reflect unsuspected functional specificities.
Genome wide analysis of common and specific stress responses in adult drosophila melanogaster.
Sex, Age, Compound, Time
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Role of Tet1/3 Genes and Chromatin Remodeling Genes in Cerebellar Circuit Formation.
Specimen part
View SamplesTranscriptome analysis of mRNA samples purified from developing cerebellar granule cells and ES cell-derived granule cells using translating ribosome affinity purification (TRAP) method.
Role of Tet1/3 Genes and Chromatin Remodeling Genes in Cerebellar Circuit Formation.
Specimen part
View SamplesBackground. Primary cilia (PC) are solitary antennae present at the cell surface. These non-motile cilia play an important role in organ development and tissue homeostasis through the transduction of the Hedgehog (Hh) signaling pathway. We recently revealed the presence of PC in the epithelium of the developing epididymis, an organ of the male reproductive system whose dysfunction triggers male infertility. Acknowledging that systemic blockade of the Hh pathway trigger epididymal dysfunctions in vivo, our main goals were 1) to portray the epididymal Hh environment, 2) to determine the direct responsiveness of epididymal epithelial cells to Hh, and 3) to define the contribution of PC to the transduction of this pathway. Results. The Hh ligands Indian and Sonic hedgehog (Ihh and Shh) were respectively located in principal and clear cells of the mouse epididymis by immunofluorescent staining. The propensity of epididymal principal cells to respond to Hh signaling was assessed on immortalized epididymal DC2 cells by western-blot, confocal imaging and 3D-reconstruction. Our results indicate that epididymal principal cells secrete Ihh and expose PC that co-localize with the conventional acetylated tubulin/Arl13b ciliary markers, as well as with GLI3 Hh signaling factor. Gene expression microarray profiling indicated that the expression of 43 and 248 genes was respectively and significantly modified following pharmacological treatment of DC2 cells with the Hh agonist SAG (250 nM) or the Hh antagonist cyclopamine (20 µM) compared with the control. Among Hh target genes identified, 6.7 % presented perfect matches for GLI-transcription factor consensus sequences, and the majority belonged to interferon-dependent immune response and lipocalin 2 pathways. Finally, the contribution of epididymal PC to the transduction of canonical Hh pathway was validated by ciliobrevinD treatment, which induced a significant decrease of PC length and the expressional reduction of Hh signalling targets. Conclusions. All together our data indicate that PC from epithelial principal cells regulate gene expression profile through a possible autocrine Hh signaling. This provides new hypotheses regarding the potential contribution of PC and Hh signaling in intercellular cross-talk and immunological regulation of the epididymis.
Hedgehog signaling pathway regulates gene expression profile of epididymal principal cells through the primary cilium.
Cell line, Treatment
View SamplesHigh endothelial venules (HEVs) are specialized blood vessels allowing recirculation of naïve lymphocytes through lymphoid organs. Here, using full length single-cell RNA sequencing, RNA-FISH, flow cytometry and immunohistofluorescence, we reveal the heterogeneity of HEVs in adult mouse peripheral lymph nodes (PLNs) under conditions of homeostasis, antigenic stimulation and after inhibition of lymphotoxin-b receptor (LTbR) signaling. We demonstrate that HEV endothelial cells are in an activated state during homeostasis, and we identify the genes characteristic of the differentiated HEV phenotype. We show that LTbR signaling regulates many HEV genes and pathways in resting PLNs, and that immune stimulation induces a global and temporary inflammatory phenotype in HEVs without compromising their ability to recruit naïve lymphocytes. Most importantly, we uncover differences in the regulation of genes controlling lymphocyte trafficking, Glycam1, Fut7, Gcnt1, Chst4, B3gnt3 and Ccl21a, that have implications for HEV function and regulation in health and disease. Overall design: Comparison of High Endothelial Cells and Blood Endothelial Cells from mouse lymph nodes under 4 different conditions with a total of 220 single cells.
Single-Cell Analysis Reveals Heterogeneity of High Endothelial Venules and Different Regulation of Genes Controlling Lymphocyte Entry to Lymph Nodes.
Specimen part, Cell line, Subject
View SamplesWe assessed the gene expression profile of purified CD205+CD8+ Dendritic Cells isolated from murine spleens.
NOD2 modulates immune tolerance via the GM-CSF-dependent generation of CD103<sup>+</sup> dendritic cells.
Sex, Age, Specimen part
View SamplesSETD5 gene mutations have been identified as a frequent cause of idiopathic intellectual disability. Here we show that Setd5 haploinsufficient mice present developmental defects such as abnormal brain to body weight ratio and neural crest defect associated phenotypes. Furthermore, Setd5 mutant mice show impairments in cognitive tasks, enhanced long-term potentiation, delayed ontogenetic profile of ultrasonic vocalisation and behavioural inflexibility. Behavioural issues are accompanied by abnormal expression of postsynaptic density proteins previously associated with cognition. Our data suggest that Setd5 might regulate RNA polymerase II dynamics and gene transcription during development and learning via its interaction with the Hdac3 and Paf1 complexes. Our results emphasize the decisive role of Setd5 in a biological pathway found to be disrupted in intellectual disability and autism spectrum disorder patients. Overall design: RNA-sequencing for wild type and Setd5 heterozygous knockout mice in two settings. First, in whole embryo samples (age E9.5), three biological replicates each. Second, gene expression changes due to contextual fear conditioning (CFC) was studied by comparing baseline transcription in homecage (HC) mice with transcription one hour (CFC_1h) or three hours (CFC_3h) after fear conditioning (4-5 biological replicates per time point and genotype).
Haploinsufficiency of the intellectual disability gene SETD5 disturbs developmental gene expression and cognition.
Specimen part, Cell line, Subject
View SamplesSepsis is a major health concern, with high morbidity and mortality workdwide. In order to identify prognostic biomarkers in septic shock patients, we performed a microarray study exploring the early modulation of gene expression according to day 28 mortality.
Modulation of LILRB2 protein and mRNA expressions in septic shock patients and after ex vivo lipopolysaccharide stimulation.
Sex, Age, Time
View SamplesWe collected tissues from bent cotyledon stage zygotic embryos, proliferating tissue at day 7 and day 14 induction of somatic embryogenesis and mature somatic emrbyos in a wild type (Col-0) and vtc2 (SALK_146824) insertion.
Vitamin C deficiency improves somatic embryo development through distinct gene regulatory networks in Arabidopsis.
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View SamplesThese arrays are used for various projects
DNA amplification is a ubiquitous mechanism of oncogene activation in lung and other cancers.
Sex, Age, Race
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